General anesthesia is antagonized by a pressure of 150 to 200 atm. The pressure antagonism indicates that the volume of the anesthetized state is larger than the awake state. We hypothesize that volume change arises mainly from a transition of a cluster of water molecules at the vicinity of the membrane changing cooperatively between two states, i.e., condensed state of electrostriction and expanded state of anesthesia. Our hypothesis predicts that anesthetics decrease membrane surface charges and dissociate water molecules from the membrane. We propose to evaluate our hypothesis on the above two points with phospholipid bilayer and monolayer model membranes. Although these models only represent part of the characteristics of cell membranes, they are chosen because quantitative thermodynamic and kinetic data are obtainable and can be analyzed rigorously. The information on electrostatic charges will be obtained by measuring surface potential (delta V) of monolayers. The electrokinetic data will be collected by measuring slipping plane zeta potential by electrophoresis of bilayer vesicles. The surface charge density will be estimated by solving the Gouy-Chapman equation. Association of water molecules will be estimated mainly by a surface viscometry. The contribution of dragging water molecules to surface viscosity will be calculated from the temperature coefficient by applying the theory of absolute reaction rate. Nuclear magnetic resonance spectroscopy will be used to study the perturbation of the structure and conformation of the phospholipid bilayer by anesthetics at at molecular level. Information on the bound water molecules is also obtainable by this method. The perturbation of the membrane caused by anesthetics will be expressed in thermodynamic functions.